Amazing Design in the Chemistry of Pregnancy

by
Brian Thomas, M.S. *

The onset of pregnancy presents an apparent contradiction. Ovulating and initially pregnant mothers experience an increase in progesterone. On the one hand, this hormone signals the immune system to back down and lay low. That's critical, because otherwise her body would fight and kill sperm cells as though they were unwelcome invaders, and she would never become pregnant.

But on the other hand, progesterone reduces cholesterol levels in her body. Too much progesterone would doom a developing baby, who requires cholesterol. Why would one action both promote and prevent a single outcome? Two University of California evolutionary biologists believe they have decoded the answer.

Publishing in the June 2013 issue of The Quarterly Review of Biology, the authors first noted that many infections, caused by both viruses and bacteria, either depend on or are enhanced by cholesterol-containing "lipid rafts" embedded on cell membranes.1 The invaders link to the lipids, using them as doors to access and infect cells, causing disease.

Normally, a woman's immune system provides plenty of protection from such potential pathogens, but when her progesterone levels rise, her immune system diminishes, making her more susceptible to disease (while making her susceptible to pregnancy). By decreasing cholesterol levels at the same time as decreasing immune response, her body shrinks the number of doors available to potential invaders—and she and her baby remain protected.

Early in the first trimester, the baby is so small that its greatest need is for a healthy mother. Later during pregnancy, progesterone levels drop, and this enables both the mother's immune system and her tiny baby's required supply of cholesterol to ramp up at the perfect pace.

The study authors wrote, "Cholesterol modulation appears to be exquisitely timed over the course of pregnancy, closely matching the shifting importance of combating pathogens and building fetal tissue."1 How did this exquisite timing arise?2

The Quarterly Review authors explain that it arose as "a second-order adaptation selected for by the increased vulnerability to infection that is an inherent consequence of progesterone's role in maternal immune tolerance of the conceptus [tiny baby]."1 Did these authors mean to say that the risk of illness literally selected the fine-tuned and exquisitely timed hormonal communication apparatus, complete with its ability to temporarily yet precisely manage the manufacture and retention rates of specific and critical biochemicals like cholesterol?

Such a claim would not be scientific unless they measured or somehow witnessed the effects of "vulnerability to infection" on an animal that does not yet have an endocrine system because the creature and its systems are still evolving. They did no such tests, since animals already have the completed endocrine systems that their bodies require. The researchers did witness the exquisite physiology already woven into mothers' bodies.

How can the ultimate origins of the endocrine system's perfectly fine-tuned timing, and its interdependent processes, be attributed to its need to avoid disease, and how could it have engineered its own intricate disease-mediating strategies without outside intelligent input? The authors' lengthy paper does not address these foundational questions. Perhaps future research will.3

Because this particular body system is so clearly the product of purposeful design, the Creator—not nature—should get the credit for originally inventing the "exquisitely timed" hormones required for human reproduction. By describing this new aspect of maternal physiology, evolutionary scientists reveal another wonder to which the psalmist referred when writing that the human body is "fearfully and wonderfully made."4

More specifically, what is the ultimate origin of this exquisite timing, notwithstanding any modifications it may have suffered since creation and the fall?

And if it does, it should also explain the origins of the precision and specificity coordinated across body tissues and the body's biochemistry during hormonal communication. This suite of well-matched endocrine parts, where the removal of one part crashes the entire human system, might require hundreds of simultaneous, perfectly engineered mutations. Accordingly, it should explain how the suite of mutations required to generate receptor proteins and feedback networks would have to simultaneously arise in both a husband's and wife's germ cells. Also, how would just their offspring's genotype come to dominate the entire human population?